Abstract
Researchers have a range of animal models in which to study Nonalcoholic fatty liver disease (NAFLD). Induction of NAFLD by a high-fat diet in the C57BL/6 strain is the most widely used among mice. In this study, we review works that performed NAFLD induction by a high-fat diet using the C57BL/6 strain, focusing on experiments on the effects of lipid ingestion. Studies are initially distinguished into researches in which mice received lipids by oral gavage and studies in which lipid was added to the diet, and each of these designs has peculiarities that must be considered. Oral gavage can be stressful for animals and needs trained handlers but allows accurate control of the dose administered. The addition of oils to the diet can prevent stress caused to mice by gavage, but possible changes in the consistency, taste, and smell of the diet should be considered. Regarding the experimental design, some variables, such as animal sex, treatment time, and diet-related variables, appear to have a definite pattern. However, no pattern was found regarding the number of animals per group, age at the beginning of the experiment, time of adaptation, the substance used as a vehicle, and substance used as a control.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is the presence of hepatic steatosis at a level greater than or equal to 5% of the liver area without the presence of other diseases that affect the organ or the use of alcohol in quantities considered harmful [1]
The presence of the disease is correlated with obesity and is present in up to 91% of severely obese patients (Body mass index—BMI > 35 kg/m2 ) [7]
We focus on NAFLD induction by a high-fat diet in C57BL/6 strain mice, which is the most commonly used strain for this experimental disease model [18]
Summary
Nonalcoholic fatty liver disease (NAFLD) is the presence of hepatic steatosis at a level greater than or equal to 5% of the liver area without the presence of other diseases that affect the organ or the use of alcohol in quantities considered harmful [1]. The spectrum of the disease ranges from simple liver fat accumulation—so-called hepatic steatosis—to more severe progressions such as nonalcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. Because some patients do not show changes in blood tests, the prevalence of the disease may be even higher [3]. The presence of the disease is correlated with obesity and is present in up to 91% of severely obese patients (Body mass index—BMI > 35 kg/m2 ) [7]
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